• Journal of Periodontal and Implant Science
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• 제43권1호
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• pp.3-11
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• 2013

Periodontitis is a chronic inflammation of periodontal tissue caused by subgingival plaque-associated bacteria. Periodontitis has long been understood to be the result of an excessive host response to plaque bacteria. In addition, periodontal pathogens have been regarded as the causative agents that induce a hyperinflammatory response from the host. In this brief review, host-microbe interaction of nonperiodontopathic versus periodontopathic bacteria with innate immune components encountered in the gingival sulcus will be described. In particular, we will describe the susceptibility of these microbes to antimicrobial peptides (AMPs) and phagocytosis by neutrophils, the induction of tissue-destructive mediators from neutrophils, the induction of AMPs and interleukin (IL)-8 from gingival epithelial cells, and the pattern recognition receptors that mediate the regulation of AMPs and IL-8 in gingival epithelial cells. This review indicates that true periodontal pathogens are poor activators/suppressors of a host immune response, and they evade host defense mechanisms.

• 미생물과산업
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• 제16권3호
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• pp.2-5
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• 1990

IgA is the predominant immunoglobulin isotype in mucosal secretions(1). It has been reported that a population of Peyer's patch T cells can selectively induce IgM bearing B cells to switch to surface IgA bearing B cells(2,3). Further, IL-4, IL-5, and IL-6 alone and in combination, can significantly influence murine IgA B cell differentiation in vitro(4-7). However, it remains an open question which cytokines have a major role in class switching to the IgA isotype. Recently, it has been reported that transforming growth factor .betha.1(TGF .betha.1) alone, or in combination with IL-2 increases IgA secretion by LPS-activated surface IgA negative (sIgA$\^$-/) murine spleen B cells while concurrently downregulating IgM and IgG secretion by such cells(8-11). In the present study, limiting dilution analysis was used to demonstrate, at the clonal level, that TGF .betha.1 has siginificant activity as an IgA isotype switch factor.

• 대한한의학회지
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• 제26권4호
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• pp.1-11
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• 2005

This study was to investigate the effect of Danchunwhangagam(DCWGG) extract on the production of proinflammatory cytokines in peripheral blood mononuclear cells (PBMCs) from Cerebral infarction(CI) patients. Methods: We examined how the inhibition rate of tumor necrosis factor (TNF)-$\alpha$, interleukin(IL)-1$\alpha$, IL-1$\beta$, IL-6, and IL-8 productions in DCWGG pretreatment PBMCs culture supernatant in the lipopolysaccaride(LPS)- or desferrioxamine(DFX)treated cells compared to unstimulated cells. Results: DCWGG inhibited the productions of TNF-$\alpha$, IL-1$\alpha$, IL-1$\beta$, IL-6, and IL-8 induced by LPS in a dose-dependent manner. Conclusions: DCWGG might have regulatory effects on LPS or DFX-induced cytokine production, which might explain its beneficial effect in the treatment of CI.

• Preventive Nutrition and Food Science
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• 제22권2호
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• pp.100-106
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• 2017

To elucidate new biological ingredients in cold-brew coffee extracted with cold water, crude polysaccharide (CCP-0) was isolated by ethanol precipitation, and its immune-stimulating activities were assayed. CCP-0 mainly comprised galactose (53.6%), mannose (15.7%), arabinose (11.9%), and uronic acid (12.4%), suggesting that it might exist as a mixture of galactomannan and arabinogalactan. CCP-0 significantly increased cell proliferation on both murine peritoneal macrophages and splenocytes in a dose dependent manner. CCP-0 also significantly augmented nitric oxide and reactive oxygen species production by murine peritoneal macrophages. In addition, macrophages stimulated by CCP-0 enhanced production of various cytokines such as tumor necrosis factor-${\alpha}$, interleukin (IL)-6, and IL-12. In an in vitro assay for intestinal immune-modulating activity, CCP-0 showed higher bone-marrow cell-proliferation activity through Peyer's patch cells at $100{\mu}g/mL$ than the negative control. These results suggest that CCP-0 may potentially enhance macrophage functions and the intestinal immune system.

• BMB Reports
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• 제50권11호
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• pp.578-583
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• 2017

Programmed cell death-1 (PD-1) is a coinhibitory molecule and plays a pivotal role in immune regulation. Here, we demonstrate a role for PD-1 in pathogenesis of inflammatory bowel disease (IBD). Wild-type (WT) mice had severe wasting disease during experimentally induced colitis, while mice deficient for PD-1 ($PD-1^{-/-}$) did not develop colon inflammation. Interestingly, $PD-1^{-/-}$ mice cohoused with WT mice became susceptible to colitis, suggesting that resistance of $PD-1^{-/-}$ mice to colitis is dependent on their gut microbiota. 16S rRNA gene-pyrosequencing analysis showed that $PD-1^{-/-}$ mice had altered composition of gut microbiota with significant reduction in Rikenellaceae family. These altered colon bacteria of $PD-1^{-/-}$ mice induced less amount of inflammatory mediators from colon epithelial cells, including interleukin (IL)-6, and inflammatory chemokines. Taken together, our study indicates that PD-1 expression is involved in the resistance to experimental colitis through altered bacterial communities of colon.

• BMB Reports
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• 제48권11호
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• pp.624-629
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• 2015

Lysozyme protects us from the ever-present danger of bacterial infection and binds to bacterial lipopolysaccharide (LPS) with high affinity. Beyond its role in the activation of protein C, the endothelial cell protein C receptor (EPCR) plays an important role in the cytoprotective pathway. EPCR can be shed from the cell surface, which is mediated by tumor necrosis factor-α converting enzyme (TACE). However, little is known about the effects of lysozyme on EPCR shedding. We investigated this issue by monitoring the effects of lysozyme on phorbol-12-myristate 13-acetate (PMA)-, tumor necrosis factor (TNF)-α-, interleukin (IL)-1βand cecal ligation and puncture (CLP)-mediated EPCR shedding and underlying mechanism. Data demonstrate that lysozyme induced potent inhibition of PMA-, TNF-α-, IL-1β-, and CLP-induced EPCR shedding. Lysozyme also inhibited the expression and activity of PMA-induced TACE in endothelial cells. These results demonstrate the potential of lysozyme as an anti-EPCR shedding reagent against PMA-mediated and CLP-mediated EPCR shedding.

• Journal of Ginseng Research
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• 제43권2호
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• pp.172-178
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• 2019

Inflammation is an innate immune response that protects the body from pathogens, toxins, and other dangers and is initiated by recognizing pathogen-associated molecular patterns or danger-associated molecular patterns by pattern-recognition receptors expressing on or in immune cells. Intracellular pattern-recognition receptors, including nucleotide-binding oligomerization domain-like receptors (NLRs), absent in melanoma 2, and cysteine aspartate-specific protease (caspase)-4/5/11 recognize various pathogen-associated molecular patterns and danger-associated molecular patterns and assemble protein complexes called "inflammasomes." These complexes induce inflammatory responses by activating a downstream effector, caspase-1, leading to gasdermin D-mediated pyroptosis and the secretion of proinflammatory cytokines, such as interleukin $(IL)-1{\beta}$ and IL-18. Ginsenosides are natural steroid glycosides and triterpene saponins found exclusively in the plant genus Panax. Various ginsenosides have been identified, and their abilities to regulate inflammatory responses have been evaluated. These studies have suggested a link between ginsenosides and inflammasome activation in inflammatory responses. Some types of ginsenosides, including Rh1, Rg3, Rb1, compound K, chikusetsu saponin IVa, Rg5, and Rg1, have been clearly demonstrated to inhibit inflammatory responses by suppressing the activation of various inflammasomes, including the NLRP3, NLRP1, and absent in melanoma 2 inflammasomes. Ginsenosides have also been shown to inhibit caspase-1 and to decrease the expression of $IL-1{\beta}$ and IL-18. Given this body of evidence, the functional relationship between ginsenosides and inflammasome activation provides new insight into the understanding of the molecular mechanisms of ginsenoside-mediated antiinflammatory actions. This relationship also has applications regarding the development of antiinflammatory remedies by ginsenoside-mediated targeting of inflammasomes, which could be used to prevent and treat inflammatory diseases.

• BMB Reports
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• 제54권11호
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• pp.545-550
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• 2021

Anisomycin is known to inhibit eukaryotic protein synthesis and has been established as an antibiotic and anticancer drug. However, the molecular targets of anisomycin and its mechanism of action have not been explained in macrophages. Here, we demonstrated the anti-inflammatory effects of anisomycin both in vivo and in vitro. We found that anisomycin decreased the mortality rate of macrophages in cecal ligation and puncture (CLP)- and lipopolysaccharide (LPS)-induced acute sepsis. It also declined the gene expression of proinflammatory mediators such as inducible nitric oxide synthase, tumor necrosis factor-α, and interleukin-1β as well as the nitric oxide and proinflammatory cytokines production in macrophages subjected to LPS-induced acute sepsis. Furthermore, anisomycin attenuated nuclear factor (NF)-κB activation in LPS-induced macrophages, which correlated with the inhibition of phosphorylation of NF-κB-inducing kinase and IκB kinase, phosphorylation and IκBα proteolytic degradation, and NF-κB p65 subunit nuclear translocation. These results suggest that anisomycin prevented acute inflammation by inhibiting NF-κB-related inflammatory gene expression and could be a potential therapeutic candidate for sepsis.

• 대한예방한의학회지
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• 제27권3호
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• pp.35-46
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• 2023

Objectives : Gumiganghwal-tang and its main components have been used for treatment of cough, headache, joint pain and fever. Using a respiratory inflammatory model, we intend to demonstrate the its anti-inflammatory effect and immune mechanism of Gumiganghwal-tang. Methods : We induced the respiratory inflammation mouse model by papain treatment. Female BALB/C mice (8 weeks old) were divided into three groups as follows: saline control group, papain treatment group (vehicle), papain and Gumiganghwal-tang (200 mg/kg) treatment group (n=4). To verify the anti-inflammatory effect of Gumiganghwal-tang extracts, we measured the infiltration of inflammatory cells in bronchoalveolar lavage fluid (BALF) and nasal lavage fluid (NALF). Additionally, the efficacy of Gumiganghwal-tang extracts on Th2 cell population and alveolar macrophage in lung were analyzed by using flow cytometry. Results : Gumiganghwal-tang extracts administration decreased inflammatory cell infiltration in BALF and NALF, especially of eosinophils. Furthermore, interleukin-5 level was reduced in lung by drug administration. Interestingly, Gumiganghwal-tang extracts treatment also decreased the Th2 cell (CD4⁺GATA3⁺) population and increased the alveolar macrophage (CD11b⁺CD11c⁺) population in lung. Conclusions : Our findings indicate that Gumiganghwal-tang extracts have anti-inflammatory effects by mediating Th2 cell and alveolar macrophage cell activation.

• Nutrition Research and Practice
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• 제11권1호
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• pp.11-16
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• 2017

BACKGROUND/OBJECTIVES: Helicobacter pylori (H. pylori) colonization of the stomach mucosa and duodenum is the major cause of acute and chronic gastroduodenal pathology in humans. Efforts to find effective anti-bacterial strategies against H. pylori for the non-antibiotic control of H. pylori infection are urgently required. In this study, we used whey to prepare glycomacropeptide (GMP), from which sialic acid (G-SA) was enzymatically isolated. We investigated the anti-bacterial effects of G-SA against H. pylori in vitro and in an H. pylori-infected murine model. MATERIALS/METHODS: The anti-bacterial activity of G-SA was measured in vitro using the macrodilution method, and interleukin-8 (IL-8) production was measured in H. pylori and AGS cell co-cultures by ELISA. For in vivo study, G-SA 5 g/kg body weight (bw)/day and H. pylori were administered to mice three times over one week. After one week, G-SA 5 g/kg bw/day alone was administered every day for one week. Tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$), IL-$1{\beta}$, IL-6, and IL-10 levels were measured by ELISA to determine the anti-inflammatory effects of G-SA. In addition, real-time PCR was performed to measure the genetic expression of cytotoxin-associated gene A (cagA). RESULTS: G-SA inhibited the growth of H. pylori and suppressed IL-8 production in H. pylori and in AGS cell co-cultures in vitro. In the in vivo assay, administration of G-SA reduced levels of IL-$1{\beta}$ and IL-6 pro-inflammatory cytokines whereas IL-10 level increased. Also, G-SA suppressed the expression of cagA in the stomach of H. pylori-infected mice. CONCLUSION: G-SA possesses anti-H. pylori activity as well as an anti-H. pylori-induced gastric inflammatory effect in an experimental H. pylori-infected murine model. G-SA has potential as an alternative to antibiotics for the prevention of H. pylori infection and H. pylori-induced gastric disease prevention.